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Antibiotics; How Do They Work?

Monday, 04 October 2010 by | Comments: 3
Reading Time: 2 minutes

Nutritional orientated practitioners are well aware of the potentially damaging effects of inappropriate prescribing of antibiotics, not simply in terms of increasing resistance but also because even a single treatment can alter the microbial ecology in the gut for months without relevant interventions.

Antiobiotics have undoubtedly been a fantastic intervention, the discovery of the sulfa drugs in the 1930 s and the subsequent development of penicillin during World War II ushered in a new era in the treatment of infectious diseases. Infections that were common causes of death and disease in the pre-antibiotic era – rheumatic fever, syphilis, cellulitis and bacterial pneumonia – became treatable, and over the next 20 years most of the classes of antibiotics that find clinical use today were discovered and changed medicine in a profound way.[i]

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Most clinically useful antibiotics exhibit their selective toxicity by specifically blocking one or another type of bacterial macromolecular synthesis (e.g.protein, nucleic acid or cell wall synthesis) — acting on targets that are not present or accessible in animal/human cells. Since the 1940s, when drugs such as penicillin, streptomycin, and chloramphenicol were introduced widely as “miraculous” agents for treating bacterial infections, the emergence of strains resistant to these and subsequently-developed drugs has represented a continuing clinical challenge. The eventual appearance of strains simultaneously resistant to multiple antibiotics significantly worsened the problem. The latter was found to involve different resistance genes linked to each other on segments of DNA able to move efficiently from one bacterial cell to another by phenomena known as horizontal gene transfer (HGT).

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